Clotting factor concentrates obtained from fractionated blood plasma have heretofore been utilized to intervene therapeutically with respect to patients suffering from hemophilia and other inherited bleeding disorders. Unfortunately, the otherwise salutary effects of clotting factor concentrates on the hemophiliac patient tend to be compromised as a consequence of the inordinate risk posed to the patient by the presence of hepatitis virus or other undesirable microorganisms in the concentrates. For example, commercial Factor VIII and IX concentrates are typically employed to increase the clotting ability of a hemophilia victim's blood, but these concentrates are prepared from pools of plasma contributed by thousands of donors and contain the inherent hepatitis risk of a like number of single unit transfusions. As McCullen and Zuckerman have shown, see Journal of Medical Virology, Vol. 8, No. 29 (1981), despite strigent screening of individual donors for hepatitis B surface antigens (HBsAg), such plasma pools clearly transmit both hepatitis B and non-A, non-B hepatitis.
Hepatitis transmission by albumin and other heat-stable plasma components unrelated to blood coagulation has heretofore been prevented by heating the plasma components in solution at temperatures of 60.degree. C. for ten hours. Similar attempts to heat clotting factor concentrates in solution, by way of contrast, have been shown to markedly reduce or eliminate clotting factor activity in the concentrates and thus do not appear to offer a viable solution to the problem of hepatitis transmission associated with conventional hemophiliac therapy. More recently, highly purified Factor VIII precipitate has been dissolved in a solution of sucrose glycine and heated for ten hours at 60.degree. C. Although the Factor VIII concentrate subsequently derived from the heated precipitate does retain clotting factor activity, the yields obtained using this approach are very low, e.g., about 8%. See Heimburger, et al., Hemostasis, Vol. 10 (supplement 1), p. 204 (1981) and Heimburger, et al., Blut, Vol. 44, p. 249-251 (1982). As a net result, the prior art to date does not furnish any means for effectively inactivating hepatitis virus present in clotting factor concentrates nor does the prior art teach a means for preventing the transmission of hepatitis virus to patients undergoing therapy with clotting factor concentrates.